Neuroimaging

‘’So how does anaesthesia really work?’’

This question has probably been asked by everyone, including those who give anaesthesia and those who receive it. While tremendous progress has been made in our understanding of the ‘mechanisms of anaesthesia’, the exact process is still unknown. As with all areas of scientific inquisitiveness, a greater understanding of the what goes on or stops in the brain during anaesthesia, would not only make us better as anaesthetists but also help develop better, more effective and safer anaesthetic drugs and techniques.

Anaesthesia induced changes in consciousness also allow us to study, possibly, the greatest scientific mystery ever, that of consciousness, itself. How different people understand and define consciousness differently reflects how little we actually understand about it. The complexities of the human brain, where different parts of the brain, specific to a certain task, interact with other areas (with other specific functions) to make us aware and conscious, are truly mind boggling.

As there are billions of nerve cells in a human brain, studying them independently is rarely possible in a living human brain. Neuroimaging provides a bridge between such microscopic brain activities and helps us interrogate the smaller macroscopic units of a living human brain.

We have set out to answer some of these questions by studying mild sedation, the first step towards unconsciousness induced by anaesthetic drugs. We use a combination of highly specialised neuroimaging tools (magneto-encephalography, electroencephalography, functional magnetic resonance imaging and spectroscopy) to explore the electrophysiological, neurochemical and blood flow changes in the brain.

Our work with propofol, one of the commonest sedative drugs, has shown that thalamus became more disconnected while the brainstem became better connected with other parts of the brain. We have also demonstrated an increase in high frequency (gamma band) oscillations induced by a visual stimulus supporting the role of an increase in inhibitory neurotransmission (GABA) at cortical or sub cortical sites with propofol.

Our current and future work will explore these findings further with sedative drugs with different mechanisms of actions to identify the commonalities of their actions.